Syntaxin 17 (D3D7H) Rabbit mAb #31261
- WB
- IP
Supporting Data
| REACTIVITY | H M R |
| SENSITIVITY | Endogenous |
| MW (kDa) | 33 |
| Source/Isotype | Rabbit IgG |
Application Key:
- WB-Western Blotting
- IP-Immunoprecipitation
Species Cross-Reactivity Key:
- H-Human
- M-Mouse
- R-Rat
Product Information
Product Usage Information
| Application | Dilution |
|---|---|
| Western Blotting | 1:1000 |
| Immunoprecipitation | 1:100 |
Storage
Protocol
Specificity / Sensitivity
Syntaxin 17 (D3D7H) Rabbit mAb recognizes endogenous levels of total syntaxin 17 protein.
Species Reactivity:
Human, Mouse, Rat
Source / Purification
Monoclonal antibody is produced by immunizing animals with a synthetic peptide corresponding to residues surrounding Val207 of human syntaxin 17 protein.
Background
Autophagy is a catabolic process for the autophagosomic-lysosomal degradation of bulk cytoplasmic contents (1,2). Autophagy is generally activated by conditions of nutrient deprivation but has also been associated with a number of physiological processes, including development, differentiation, neurodegeneration, infection, and cancer (3). Syntaxin 17/STX17 is a SNARE factor recruited to autophagosomes and required for autophagosome fusion to lysosomes. Syntaxin 17 interacts with SNAP29 (Qbc-SNARE synaptosome-associated protein 29) and the lysosomal factor VAMP8 (R-SNARE vesicle-associated membrane protein 8), as well as BRUCE, an inhibitor of apoptosis (IAP) protein, which is also involved in autophagosome/lysosome fusion (4,5).Syntaxin 17 promotes initiation of PINK1/Parkin-independent mitophagy, which is regulated by depletion of the mitochondrial outer membrane protein Fis1 (6).
- Reggiori, F. and Klionsky, D.J. (2002) Eukaryot Cell 1, 11-21.
- Codogno, P. and Meijer, A.J. (2005) Cell Death Differ 12 Suppl 2, 1509-18.
- Levine, B. and Yuan, J. (2005) J Clin Invest 115, 2679-88.
- Viret, C. and Faure, M. (2019) Trends Cell Biol 29, 1-3.
- Corona, A.K. and Jackson, W.T. (2018) Trends Cell Biol 28, 869-81.
- Xian, H. et al. (2019) Nat Commun 10, 2059.
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